title: Upregulation of TRPC1 contributes to contractile function in isoproterenol-induced hypertrophic myocardium of rat.
abstract: OBJECTIVE
  The transient receptor potential canonical channel 1 (TRPC1) is a crucial component of the stretch-activated ion channels (SACs). The objective of this research was to demonstrate the contribution of TRPC1 in maintaining cardiac contractile function in the hypertrophic myocardium.
  
  
  METHODS
  Hypertrophic rat hearts were induced by injecting isoproterenol intraperitoneally, and the expressions of TRPC1/3/6 and Na(+)/Ca(2+) exchanger 1 (NCX1) proteins were analyzed by Western blot. The intracellular calcium images, the action potential of myocardium, the length-dependent contractile force of ventricle muscle and the cardiac output of isolated heart were investigated.
  
  
  RESULTS
  The expression of TRPC1 was increased in the hypertrophic myocardium. After being stretched, the ascendant amplitude of the increase in the intracellular calcium ion concentration ([Ca(2+)]i) in the hypertrophic myocardium was higher than that in the normal myocardium. The increase of the APD50 and the amplitude of the membrane potential depolarization were more significant in the hypertrophic myocardium after the activation of SACs. When the heart preparations were perfused with Tyrode's solution, there was no difference in the cardiac systolic function between the cardiac hypertrophy group and the control group. Gadolinium, a SACs blocker, reduced the length-dependent contractile force and suppressed the ascending limb of the Frank-Starling curves in the hypertrophic heart.
  
  
  CONCLUSIONS
  The upregulation of TRPC1 contributes to the contractile function in the hypertrophic myocardium by increasing [Ca(2+)]i through the SACs.
authors.affiliation: Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, People's Republic of China.
authors.forename: Mo-Si
authors.initials: MS
authors.lastname: Chen
authors.forename: Jun-Hua
authors.initials: JH
authors.lastname: Xiao
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.forename: Bo-Ming
authors.initials: BM
authors.lastname: Xu
authors.forename: Lu
authors.initials: L
authors.lastname: Gao
authors.forename: Jia-Ling
authors.initials: JL
authors.lastname: Wang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism; D006332:Cardiomegaly / Q000139:chemically induced* / Q000378:metabolism*; D007545:Isoproterenol / Q000633:toxicity*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D050052:TRPC Cation Channels / Q000235:genetics / Q000378:metabolism*
chemical_list: D050052:TRPC Cation Channels; C096351:transient receptor potential cation channel, subfamily C, member 1; D007545:Isoproterenol; D002118:Calcium